Atrial Fibrillation Genetics Update: Toward Clinical Implementation

Kalstø, Silje Madeleine; Siland, Joylene E.; Rienstra, Michiel; Christophersen, Ingrid E.

doi:10.3389/fcvm.2019.00127

Cited by 22 publications

(11 citation statements)

References 141 publications

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“…Atrial fibrillation (AF) is caused by various mechanisms and one of the most common cardiac rhythm disturbances (Chua et al, 2019;Sutanto et al, 2019) associated with increased risk of heart failure, stroke (Kostopoulou et al, 2019), and death. More than dozens of genetic loci have been associated with AF, but the current review does not attempt to focus on these genetic mechanisms (Kalsto et al, 2019) and clinical management (Sutanto et al, 2019) of AF in detail.…”

Section: The Heart and Arrhythmiasmentioning

confidence: 99%

ArrhythmoGenoPharmacoTherapy

Tósaki

2020

Front. Pharmacol.

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This review is focusing on the understanding of various factors and components governing and controlling the occurrence of ventricular arrhythmias including (i) the role of various ion channel-related changes in the action potential (AP), (ii) electrocardiograms (ECGs), (iii) some important arrhythmogenic mediators of reperfusion, and pharmacological approaches to their attenuation. The transmembrane potential in myocardial cells is depending on the cellular concentrations of several ions including sodium, calcium, and potassium on both sides of the cell membrane and active or inactive stages of ion channels. The movements of Na + , K + , and Ca 2+ via cell membranes produce various currents that provoke AP, determining the cardiac cycle and heart function. A specific channel has its own type of gate, and it is opening and closing under specific transmembrane voltage, ionic, or metabolic conditions. APs of sinoatrial (SA) node, atrioventricular (AV) node, and Purkinje cells determine the pacemaker activity (depolarization phase 4) of the heart, leading to the surface manifestation, registration, and evaluation of ECG waves in both animal models and humans. AP and ECG changes are key factors in arrhythmogenesis, and the analysis of these changes serve for the clarification of the mechanisms of antiarrhythmic drugs. The classification of antiarrhythmic drugs may be based on their electrophysiological properties emphasizing the connection between basic electrophysiological activities and antiarrhythmic properties. The review also summarizes some important mechanisms of ventricular arrhythmias in the ischemic/ reperfused myocardium and permits an assessment of antiarrhythmic potential of drugs used for pharmacotherapy under experimental and clinical conditions.

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Section: The Heart and Arrhythmiasmentioning

confidence: 99%

ArrhythmoGenoPharmacoTherapy

Tósaki

2020

Front. Pharmacol.

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“…The diamond represents the OR and 95% CI of the pooled results. (24,25). Given more and more published studies with inconclusive results, our current study may provide some insight into further clarification of the relationship between rs13216675 and risk of AF and may direct future research to potential targets of prevention, treatment, and management of AF.…”

Section: Discussionmentioning

confidence: 83%

Association Between GJA1 rs13216675 T>C Polymorphism and Risk of Atrial Fibrillation: A Systematic Review and Meta-Analysis

Chen

Zhang

et al. 2020

Front. Cardiovasc. Med.

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Background: Rs13216675 T>C polymorphism, an SNP (single-nucleotide polymorphism) close to the gap junction protein alpha 1 (GJA1) gene, has been reported to be associated with risk of atrial fibrillation (AF); however, the results remained inconclusive. We aimed to perform a systematic review to clarify the relationship between rs13216675 and risk of AF. Materials and methods: We systematically searched the databases of PubMed, EMBASE, Web of Science, and the Chinese National Knowledge Infrastructure up to July 15, 2020. Data were synthesized using the random-effects model. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to estimate the relationship between rs13216675 and risk of AF. Results: Seven studies involving 39,827 cases and 458,466 controls were analyzed in the meta-analysis. The overall pooled OR of rs13216675 polymorphism for AF was significant (OR = 1.10, 95% CI = 1.07-1.12, P < 0.001) under the additive genetic model. Subgroup analyses revealed that rs13216675 polymorphism was significantly associated with AF in both Asians (OR = 1.12, 95% CI = 1.07-1.17, P < 0.001) and Europeans (OR = 1.09, 95% CI = 1.06-1.12, P < 0.001). When data were stratified by control sources, rs13216675 polymorphism was significantly related to AF in studies with both population-based controls (OR = 1.09, 95% CI = 1.07-1.12) and hospital-based controls (OR = 1.12, 95% CI = 1.07-1.17). No evidence of publication bias was detected. Conclusion: Our meta-analysis suggested that rs13216675 was significantly related to risk of AF and, therefore, might serve as a potential biological marker of AF.

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“…The occurrence of AF and CS can be reduced by treatment by those measures for T2D patients. However, as far as the early prevention and control of AF and CS are concerned, clinical evaluation of genetic risk is an important link in comprehensive management of AF in diabetes that cannot be ignored [ 21 ]. Like diabetes, recent genetic studies indicated that there is also an obvious genetic predisposition for the occurrence of AF [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Association of ACE2 variant rs4646188 with the risks of atrial fibrillation and cardioembolic stroke in Uygur patients with type 2 diabetes

Liu

Pei

Lai

et al. 2021

BMC Cardiovasc Disord

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Background Atrial fibrillation (AF) is the most common cardiac arrhythmia. Type 2 diabetes (T2D) is an independent risk factor for AF. The cardioembolic stroke (CS) risk is increased when both conditions coexist. Whether angiotensin-converting enzyme 2 (ACE2) genetic variants predict increased risks AF and CS in Uygur patients with T2D remain elusive. Methods A total of 547 Uygur subjects (272 controls and 275 T2D patients) were recruited to the study from south Xinjiang. Eight ACE2 variants were identified by MassARRAY system. Results ACE2 rs2074192 (CC, adjusted RR = 2.55, 95% CI 1.35–4.80, P = 0.004), rs4240157 (CC + CT, adjusted RR = 2.26, 95% CI 1.27–4.04, P = 0.006) and rs4646188 (TT, adjusted RR = 2.37, 95% CI 1.16–4.86, P = 0.018) were associated with higher AF risk. ACE2 rs4240157 (CC + CT, adjusted RR = 2.68, 95% CI 1.36–5.27, P = 0.004) and rs4646188 (TT, adjusted RR = 2.56, 95% CI 1.06–6.20, P = 0.037) were further associated with higher CS risk. The 3 ACE2 variants were related to larger left atrial end-systolic diameter (LAD) (all P < 0.05), but not all of the 3 ACE2 variants were related to increased levels of serum sodium (rs4240157 and rs4646188, all P < 0.05), HsCRP (rs4240157 and rs4646188, all P < 0.05) as well as decreased serum potassium levels (rs2074192 and rs4646188, all P < 0.05). The 3 ACE2 variants exhibited heterogeneity on circulating RAAS activation. In particular, ACE2 rs4646188 was associated with higher levels of ACE (P = 0.017 and 0.037), Ang I (P = 0.002 and 0.001), Ang II (both P < 0.001) and ALD (P = 0.005 and 0.011). Conclusion These results indicated ACE2 rs4646188 was associated with increased risk of AF and CS among diabetic patients in Uygurs, which could be a promising genetic predisposition marker for early and personalized prevention strategies for the aforementioned clinical pathologies.

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Atrial Fibrillation Genetics Update: Toward Clinical Implementation

Cited by 22 publications

References 141 publications

ArrhythmoGenoPharmacoTherapy

ArrhythmoGenoPharmacoTherapy

Association Between GJA1 rs13216675 T>C Polymorphism and Risk of Atrial Fibrillation: A Systematic Review and Meta-Analysis

Association of ACE2 variant rs4646188 with the risks of atrial fibrillation and cardioembolic stroke in Uygur patients with type 2 diabetes

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